期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 93, 期 4, 页码 537-547出版社
WILEY
DOI: 10.1189/jlb.0312169
关键词
B cell spreading; membrane-bound antigens; B cell activation; Ca2+ signal; cofilin
资金
- Hungarian National Science Fund (OTKA)
- National Development Agency (NFU) [CK80283, CK80935, CK80689]
- European Social Fund [TAMOP 4.2.1./B-09/1/KMR-2010-0003]
- Hungarian Academy of Sciences
B cells acquire membrane-bound cognate antigens from the surface of the APCs by forming an IS, similar to that seen in T cells. Recognition of membrane-bound antigens on the APCs initiates adhesion of B lymphocytes to the antigen-tethered surface, which is followed by the formation of radial lamellipodia-like structures, a process known as B cell spreading. The spreading response requires the rearrangement of the sub-membrane actin cytoskeleton and is regulated mainly via signals transmitted by the BCR. Here, we show that cytoplasmic calcium is a regulator of actin cytoskeleton dynamics in B lymphocytes. We find that BCR-induced calcium mobilization is indispensible for adhesion and spreading of B cells and that PLC gamma and CRAC-mediated calcium mobilization are critical regulators of these processes. Measuring calcium and actin dynamics in live cells, we found that a generation of actin-based membrane protrusion is strongly linked to the dynamics of a cytoplasmic-free calcium level. Finally, we demonstrate that PLC gamma and CRAC channels regulate the activity of actin-severing protein cofilin, linking BCR-induced calcium signaling to the actin dynamics. J. Leukoc. Biol. 93: 537-547; 2013.
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